In terms of positive stuff that we’re going to hopefully see at this year’s ASCO, I think a lot of people are interested in some of the smaller niche molecular abnormalities that may be targetable, so EGFR exon 20 insertions that’s maybe about 10% of EGFR mutations. We’re gonna see data with the TAC-32788 drug which is reporting about a 40 percent response rate that’s looking comparable to the poziotinib data we’ve seen before...
In terms of positive stuff that we’re going to hopefully see at this year’s ASCO, I think a lot of people are interested in some of the smaller niche molecular abnormalities that may be targetable, so EGFR exon 20 insertions that’s maybe about 10% of EGFR mutations. We’re gonna see data with the TAC-32788 drug which is reporting about a 40 percent response rate that’s looking comparable to the poziotinib data we’ve seen before. We’re gonna see updates on the LOXO drug in RET-positive non-small cell lung cancer that’s showing about a 60+% response rate, again looking like that’s gonna be a real targetable abnormality. We’ve also seen similar data with BLU-667 at AACR and I think in the immuno-oncology front two things: one is we’re going to see that chemo-immuno approach showing fruit in the squamous population which I think we’re all excited about; and perhaps the most controversial topic which is going to be in the plenary session is pembrolizumab monotherapy in those who have relatively low tumor proportion score. The question is, is it all just driven by the high TPS group relative to chemotherapy, or is there some benefit? And if it’s just kind of equivalent to chemotherapy, is that enough to shift people’s practice?
So some of the breakthroughs at this year’s ASCO are negative as much as they are positive. We’ve just come from a session which was looking at the potential of immuno-oncology PD-1 and PD-L1 antagonists to be combined with ALK inhibitors in ALK-positive lung cancer, and the results I think were very sobering. They did pretty much nothing other than add toxicity; there wasn’t a single shred of evidence that they increased efficacy. All of the efficacy looked like it was what you would get from the TKI alone, and certainly sometimes the tolerability was very poor. I think this is a field that needs to say we tried it on the basis of not very much science, and we need to move on. Maybe there are other situations where you can make these things immunogenic, but just simply combining with the tools we currently have is not the way to go.